Models for the mechanisms underlying plant-patiogen interactions have typically involved host-specific receptors that recognize pathogen-specific ligands released from the invading pathogen (Dixon et al., Annu. Rev. Phytopathiol 32:479-501, 1994; Lamb, Cell 76:419-422, 1994; Boller, Annu. Rev. Plani. Phzysiol. Plant Mol. Biol. 46:189-214, 1995). This signal transduction pathway then leads to the induction of a broad repertoire of host defense responses, including phytoalcxin biosynthesis (Keen, In: Plant Disease Control, R. C. Staple, ed, John Wiley & Sons, New York, pp. 155-177, 1981), the synthesis and secretion of hydrolytic enzymes (Kombri et al., Proc. Natl. Acad. Sci. USA 84:6750-6754, 1988), the rigidification of the plant cell wall (Bradley et al., Cell 70:21-30, 1992), and the activation of a developmental program for localized cell death. When successful, these responses ultimately arrest the growth of the invading microorganism.
In addition to pathogen-specific signals that induce host defense gene expression, there have been a number of reports suggesting that diffusible or transmissible host-derived signals are involved in orchestrating plant defense responses. For example, Dixon et al. (Plant Physiol. 71:251-256, 1983) have reported that denatured RNase was capable of inducing the release of a low molecular weight soluble factor that activates phenylpropanoid biosynthetic enzymes and phytoalexin accumulation in both soybean hypocotyls and cell suspension cultures. Graham and Graham (Plant Phzysiol. 105:571-578, 1994) have also reported that a transmissible signal, referred to as an elicitation competency factor, was released from wounded cells and was found to induce and enhance cellular responses to wounding in proximal or (closely neighboring cells. In addition, H.sub.2 O.sub.2 has been identified as a diffusible signal that is capable of selectively triggering the induction of a subclass of host defense genes (Levine et al., Cell 79:583-593, 1994).